This project is part of a long-range study aimed at identifying fundamental features of traumatic cerebral edema and testing therapeutic measures for its control. The experimental model used involves mechanical impact to the closed skulls of cats, with collection of data from animals with unilateral contusion. Recent findings from this laboratory indicate that in cerebral hemispheres with contusion, measurable cerebral edema occurs as early as 30 minutes following head trauma. Our data also suggests that the edema seen in the acute period arises from sources in addition to injured vessels in the area of contusion. The present project is designed to correlate chemical, physical, and structural data collected during the acute period following closed head trauma in order to identify events that contribute to the pathophysiology of acute traumatic cerebral edema. For this study, the following will be evaluated at 15 minutes, 2 hours, and 6 hours following head trauma: 1) intracranial pressure, systemic arterial pressure, central venous pressure, and EEG, monitored continuously and compared to preinjury values; 2) arterial blood pH, pO2, and pCO2; 3) regional brain phospholipids and free fatty acids, measured by two dimensional thin layer chromatography and gas liquid chromatography; 4) regional brain metabolites, using enzyme fluorometric techniques; 5) regional brain osmolality determined directly with a vapor pressure osmometer; 6) magnitude of brain edema, measured by change in brain density from control values; 7) alterations in the gross, light microscopic and electron microscopic morphology of the brain; and 8) location and nature of changes in cerebral vascular permeability to protein, using tracers with electron microscopy. These experiments employ established techniques for physiologic monitoring, electron microscopy, phospholipid and free fatty acid analysis, and brain metabolism, density and osmolality measurements. It is anticipated that the findings of this study will add to our understanding of the acute responses to closed head injury, the pathophysiology of traumatic cerebral edema, and the rationale for appropriate early therapy in the head-injured patient.